Paramedic 2

Start Studying!

Terms

undefined, object

copy deck

How do we classify burns in prehospital setting?: by the
Location
Depth
Surface Area
Cause
Describe a superficial burn: Top portion of epidermis
Skin is pink/red & blanches
Skin heals within 3-7 days
No permanent scarring
can be very painful
Describe a partial burn: Epidermis and part of dermis
Skin pink-red w moderate oedema
Blisters present
Adnexal struct involved, but basal layers can regrow
Extremly painful, nerve endings exposed
Can heal w 10-21 days
Describe a full thickness burn: Entire epidermis and dermis
Adnexal structs destroyed, skin cannot regenerate
skin is leathery, white or charred
Require skin grafts
nerve endings and bv destroyed
How do we calculate the SA of the burn?: Using the wallace rule of nines i pre hosp and the lund browder in hosp espec for paeds
What burns are classified as major burns?: Partial/Full thickness with:
-BSA >10% in <10 or >50 yo's
-BSA >25% in any ages
-Threat of fnal/cosmetic to face, hands, feet, genitalia
-full thickness > 5%
More major burns: -Electrical burns,incl lightening
-Chemical burns w fnal/csm threat
-Inhalational burns
-Circumferencial burns to limbs/chest
2 more major burns: -Burns pt w pre existing medical prblem that could complicate recovery/treatment
-Any burns pt with trauma
Describe Thermal burns: Most common, highest risk in 18-35 yo
high incidence of scalding in 1-5 yo
Soft tissue burnt w exposed to 45 degrees
necrosis x2 w every > of 1*
What does thermal burns do to tissue?: Causes coagulation of soft tissue, cap perm >, Oedema begins, Microemboli form from viscus plasma
fluid loss ?=> shock, hypoval
burns can > metab rate
What are the 3 zones of injry in thermal burns?: Zone 1: Zone of coagulation
-centre of wound,most intense point of contact
-tissue is coagulated and cells necrosed
Zone 2: Zone of stasis.
-surr critically inj area
-potentialy viable
-the ischemic cells here will die within 24-48 hrs
Zone 3: Zone of hyperemia
-endge of wound
-cells still alive
->bld flow due to infalmmn
-recover w 7-10 days if no inffection begins
What happens to circulation as a result of a burn?: increased evaporation=
possible burn shock can occur:
< CO, <Venous Return, > Vasc resistance
eventually:hemolysis, rhabdo,myoglobin urea,ARF, death
How do we treat thermal burns?: DANGERS- be safe!!
prim survey, VSS, sec survey
remove clothing, jewellery ect
cool for at least 20 mins,watch hypothermia tho
burns dressing
pain relief, o2,salbut if wheeze, fliuds if need
How are fliuds administered to burns patients?: Via the Parkland rule
= 4ml/kg * %BSA.
Over 24 hrs, with half given in first 8 hrs
When would you suspect airway burns?: When patient has:
hoarse voice
burns to face/lips/head
wheeze/ stridor
odema to face/airway
carbonaceous sputum
obvious resp distress
What is special about airway burns?: They account for most mortality in burns victims
they can take up to 24 hours for symptoms to be displayed
Chemical burns, acids v alkalis: Acids cause coagulation necrosis

Alkalis cuase liqufication necrosis, alkalis can also cause burns that look superficial, but spread to full thickness
How do we treat chemical burns?: Brush away as much of chemical as you can
copious irrigation
pain relief
(dont put water on Ca,Mg,Li)
Electrical burns, what are the 3 risk groups? What is severity related to?: Kids, teenagers and electrical workers.
Current type, volts, intensity, resistance, area and durn
What does an electrical burn result in?: Contact burns, thermal heating,
flash arc and flame thermal burns.
Low voltage:muscle tetany, > contact
High voltage:single violent contraction, person thrown
What are the 5 types of contact with an electrical burn?: Direct, side flash, contact, ground current, step potential.
Treatment of electrical burns?: Same as thermal,
but add monitor
IV fluids 20ml/kg bolus
musc relaxant?
watch for devel rhabdo
What are some complications of all burns?: Dehydration
infection/sepsis/tetanus
temp control issues
Scarring
Arrythmia, heart failure
pneumonia, shock, renal &liver failure
ENVIRONMENTAL EMERGENCIES: Dehydration, hypothermia, hyperthemia, frostbite
What are the four mechanisms of heat transfer?: Radiation, conduction, convection and evaporation
How is our temperature regulated?: by the thermoregulation centre in the hypothalamus. there is a heat loss centre and a heat promoting centre
What are heat promoting activities?: Vasoconstrn, >metab, >shivering, behaviour modification
What are heat loss activities?: Heat promoting centre is inhibited, heat loss centre activated
vasodilation, sweating, behaviour modification
What is fever? Why is it important?: it is controlled hyperthermia.
pyrogens act on hypothal to cause rel of prostaglandins,
> hypothal thermostat
protective mechanism to increase healing and stop bacteria.
Hyperthermia: what are the three types?: heat cramps, heat exhaustion and heat stroke
Heat cramps, describe?: sever intermittent pain, faint, dizzy, weak, hot, sweaty, tachyc
treat by removing from heat, give cool drinks
Heat exhaustion?: >in CBT: 38-40 degrees
ACS, postural hypot,dizzy, n/v, lethargey, cool pale clammy, rapid rr
treat:remove from heat, assist cooling, fliuds(oral)
Heat stroke?: SEVERE. can suffer NS dysfn
no thermoregn. tachyc/p, hot dry skin,cns dysnf,coma, seizure,coagulopathy, APO
many complications:ARF,ARDS,DIC, rhabdo.
treat:activly cool,o2,transport, dont shiver
What are the mechanisms that could cause hypothermia?: < heat production(hypoglyc, malnutrition)
inapprop heat regn(cns disease, poison)
> heat loss(cold exposure)
< activity (elderly)
What is the process of hypothermia?: bw 37-35:shivering,numb,clumsy <mental processing(34:compensation stops here.ie >RR,HR,BP stop)
33-30:drowsy, shiver stops, rigid, blue, hallcinate
29:unconc
23:heart stops
How do we manage a hypothermic patient?: if no pulse just ventilate 6-8/min, NO CPR(<mvt or get VT)
warmd o2 if poss, posn on back, wrap up, provde hot env, warm fluids(dextrose) transport!
Frostbite, process?: get in freezing, wet, windy env
skin red inflamed=>grey wax like
pain, numbness,stinging,blisters
blackening of skin
remove from cold,ensure good circn, hot sweet drinks, pain relief
Barotrauma: what is it?: The compression or expansion of gases in the body when the pressure in body differs from ambient environment.
Barotrauma of descent: Air trapped in non collapsable containers in compressed:vacume type effect.
causes sharp pain, blocked nasal tubes,headace,vertigo,SOB, nose/ear bld.
Barotrauma of Ascent: As diver ascends, gas trapped in tissues/bld, it cant escape, so expands in tissues.
get POPS:alveoli rupture
subcutaneous emphys, pneumoth, pneumocardium, pneumoperitoeum
Air embolism: Suspect in anyone who goes unconc after diving! air gets trapped in small cicrn causing vertigo, confusion, visual dist, LOC (smiliar in presentn to stroke)
Decompression sickness: nitrgoen bubbles forming in bld as diver ascends.s/s presnt 6-48 hrs following dive.
s/s:pain, neuro dysfn, ACS
magmt:O2 IV if need, pain relief ?, transp for hyperbraic treamnt
Nitrogen narcosis: N dissolves in bld at depth and crosses BBB. has depressive effect,effects all divers, experience helps cope.
Altitude illness: due to different partial pressure of o2
=hypobaric hypoxia
what is the pathopys of hypobaric hypoxia?: Increase in cerebral bf, causes increas in cerbral capil pressure, > capill permeab leads to CEREBRAL ODEMA
also stims SNS response(>fluid)
Acute Mountain Sickness AMS: Ascending too rapidly,devel w 4-6 hrs. abates after 3-4 days
s/s lightheaded, SOB, tachyc, hypot, 'hangover', ataxia, > RR due to hypoxia
High Altitude Pulmonary Oedema HAPO: Most lethal.
s/s dry cough, tachyc/p, cyanosed,weak, rales =>ACS, coma, death
treat w 100% o2, descent, hyperbaric treatment
High Altitude Cerebral odema HACO: Is extreme progression of AMS, leads to increase of ICP
s/s:ACS=> coma
Mgmt: 100% o2, descent
Hyperbraic therapy: Increases partial pressure of 02 and pressure of 'air'.
for:severe bld loss anaemia
:crush inj/ compartment syndr
:decomp sickness
effects of hyperbaric treament: increases o2 into tissues,
can help with AMI, CVA, musc neuro disease
Toxicology Iron poisoning: very corrosive to GIT
vomiting
diarrhea
abdo pain
ulceration
GI bleeding
What are the five stages in iron poisoning?: Stage 1:direct irritation of GI
n/v, abdo pain, diahrrea
Stage 2: 6-12 hrs after: feel 'better' metabolic abnormalities still present
Stage 3 and 4: Stage 3: Metabolic acidosis
shock, acidosis, coagulopathy, liver dysfn
Stage 4:2-5 days after
possible liver failure
Stage 5:: Scarring of GIT, stomach and intestine are effected.
Treatment of iron poisoning: O2, monitor, 2 IV, Hartmanns 20ml/kg and maxalon
Hdrocarbons: Pulmonary toxicity, CNS toxicity, demylination of nerves, blood, heart and skin toxicity
Organophosphate posioning: pesticides, absorbed, inhaled, ingested. OPs work on inhibiting AChE, so there is an increase in ACh in nerve synapses.
Signs and symptoms: Muscarinic and nicotinic overstimulation.
=slud, GI cramps, n/v, bronchospasm, bradycardia blurred vision, ACS, dizzy, seizure, hypot
Management:: decontaminate-remove everything, poisoning will continue if not alert ED
DRABC etc
Iv access
ATROPINE 1.2mg every 5 mins
Pyrethrin: 'safest insecticide'
allergic response common
Rhodenticides: many types, eg superwarfarins
s/s:lactic acidosis, n/v, GI heam, pain, parenthesias,wkness, tremor, seizure
Cyanide: stops ATP production, metabolic acidosis.
mucous membr irritatn, anxiety, headache, dyspnea, confusion, seizure, coma, death
red skin
Managemnt of Cyanide poisoning: DRABC, 100% o2, decontaminate monitor, iv hartmanns, transport and notify
Paracetamol: produces a toxic byproduct that kills liver cells
Codine: chemically rel to morhpine
:ACS, <GCS, < airway mechs
S/S n/v, drowzy, < resp, pinpoint pupils, hypot
Cough syrup: > doses cause narcotic overdose
resp <, ACS, drowsy
Decongestants: induce vasoconstrn by stimuln of alpha receps
s/s hypert, headache, resp distress, insomnia, agiation, tachyc
NSAIDs: Increase GI bleeding and renal failure
S/S: n/v, abdo pain, CNS changes, seizure? hypot?
Aspirin: salicylate, toxicity deps on cellular concentrn
causes resp alkalosis, > catabolism, metab acidosis
Tricyclic antidepressents: relate to antmuscarinic and antihistamine effects
S/S: drowsy, ataxic, ECG changes, APO, aspirn pneum, hyperthermia, rhabdo
drug of choice to treat: sodium bic
Envenomation notes. what is the main actions of venom?: To paralyze prey
by: interfering with neuronal conduction, junction transmissionm muscular contractions
Australian snakes: Elapids, use the lymphatic system to distribute their venom
What is in venom?: Prothrombin aciviting enzymes which produce thrombin
peptides that block skel muscl ach channels
What are the effects of venom?: Haemotoxic
Myotoxic
Neurotoxic
Haemolytic
what effects does elapid venom have on blood?: Can inhibit plasmin that degrades fibrin; can cause DIC
S/S: bite site us painless
not always teeth marks, can be scratches
bruising, bleeding, swelling
when should you consider snake bite: unexpextd confusion/LOC after outdoor activites
more s/s?: Cardiac depression
paralysis
DIC/coagulopathy?
?haematuria, haematemesis(20% victims have cerebral haemorr)
How do S/S progress?: Highly variable
headache, n/v, confn, diarrhea, coaguln
paralysis, pain, hypert, tachyc
resp failure, circ failure
How can you treat snake bite?: lymph system transports venom
firm bandage and immoblisn will < flow of venom
can get venom detection kits to det what anitvenom to use
Blue bottle jellyfish: sharp instant pain, becomes violent aching pain
possible headache, vomiting, abdo cramps, ACS, collapse
Mgmt:: remover tentacles, use cold water and ice packs
apply lignocaine cream(use penthrane/morph if need)
Box jellyfish, how do they sting and whats in their toxin?: Most dangerous.
tentacles covered with nematocytes, discharge toxins into skin
toxin:haemolytic, cardiotoxic,dermanecrotic
What does the toxin do to you?: heart becomes stuck in systole, bradycardia may devel, respir arest, bp changes, musc contrn, haemolytic
what are the S/S?: immediate pain,
tentacles may stick to skin
weals devel,infalm, and oedematous
if severe:hypot, dysryth, apnoea
Magmt:: remover from water
pour vinegar on to inactivate tentacles
DONT PRESSURE IMMOBLISE
Blue ringed octopus, what does their saliva contain?: different toxins that can:
block neuromuscular transmission, cause < bp
S/s?: Weakness, numbness around face and neck
difficulty breathing
N/v
+/- bradyc, hypot
can progress to ACS, ataxia
Mgmt blue ringed octopus?: pressure immob
O2
pain relief if need
rapid transport
stingray s/s?: puncture/lacs, pain increases over time,
wound will bleed, then turns blue/white colour
n/v, sweating, musc cramps, poss ACS, seizure
infection is common complic
mgmt?: control haemrr. pain relief(topical is best)
transport
Stone fish, effects of venom?: most dangerous venomous fish
< of CV and Nueromusc syst, direct effect on muscle fn
haemolysis, > vasc permeab
treat: warm water, no press/immb
Sea snakes, what does the venom do?: painless bite
causing periph paralysis, musc necrosis
doesnt effect blood
Sea urchins, what does the venom do?: causes an anaphlyactic type response, ie < bp, swelling, < respir, rash, sweating, tachy
Manage?: o2 pain relief(-but dont want vasodiln)
pressure immob,
+/- adenaline to help w hypot
Cone shells S/S?: swelling, burning, small wound, bruises fast
numbness,
nausea
Malaise, wkness, ACS, SOB
Spiders, venom effects?: nuerotoxic, CV effects, pulm odema, metabolic acidosis, hyperthermia
Gen S/S?: n/v, pain, swelling, odema,
sweaing, lacrimation
dyspnea
ACS, paralysis, tachyc

Start Studying!

Deck Info

Number of cards 100